Urban living, industrial employment and cigarette smoking bring man into daily contact with carbon monoxide (CO). Our early work shows that high sublethal levels of CO can induce polycythemia and cardiac enlargement during chronic exposure. More recent studies show that prolonged CO poisoning produces alterations in cardiac lactate dehydrogenase isozyme pattern and myocardial ultrastructure. It is now clear from studies with isolated right ventricle and left ventricle preparations that prolonged CO exposure also compromises aerobic contractile performance; the longer the exposure the greater the performance decrement. However, such CO exposure also produces an enhanced tolerance of anoxia and an increased ability to recover function in oxygen following a period of anoxia. We intend to proceed further by investigating heart function in the CO exposed animal by use of the isolated papillary muscle and in situ through use of implanted catheters and flow probes on the heart. Another area of investigation now being initiated is examination of the regression of various CO-induced effects following cessation of CO exposure. Does the animal become essentially normal once again? Yet another area involves examining the mode of cardiac enlargement during CO exposure (true "hypertrophy" vs. hyperplasia) in animals of different ages. Finally a project is just now beginning to look at changes in mitochondrial oxidative capacity (via cytochrome c and e.m. morphometric techniques) and myofibrillar ATPase in animals exposed to CO. This work will enhance our understanding of the range of adaptive/pathological responses of heart to chronic stress. BIBLIOGRAPHIC REFERENCES: D. Penney, M. Benjamin and L. Bugaisky (1975) Cardiac anoxia tolerance of carbon monoxide-poisoned, hypoxia exposed and normal rats. Environmental Physiol. & Biochem. 5, 127-131. D. Penney and M. Thomas (1975) Hematological alterations and response to acute hypobaric stress. J. Appl. Physiol. 39,1034-1037.